The principal objective of our proposed research is to study immunologic escape mechanisms in prostatic carcinoma, especially suppressor T cell activity. We will also investigate the role of serum factors that either block at the tumor cell level or inhibit at the effector cell level. Because many of the experimental manipulations necessary for the proper study of tumor systems cannot, for ethical reasons, be performed in humans, we intend to utilize an animal model that mimics the human condition. The R3327 tumor is unique among animal models in terms of its similarity to human prostatic carcinoma. Before we can study immunologic escape mechanisms, it is essential that we first establish that the R3327 tumor is, in fact, immunogenic. We intend to do this by using classical in vivo transplantation resistance and adoptive transfer experiments. To apply these studies to the human condition, we will need to correlate results of in vivo experiments that can be done only in experimental animals with in vitro assays that can be performed in both animals and humans. We intend to use several in vitro assays that have been reported to reflect tumorimmune responses including, the (1) mixed lymphocyte-tumor cell interaction, (2) the leukocyte adherence inhibition assay, and (3) cellular and humoral cytotoxicity assays.. It is our intention to determine which of these in vitro assays correlate best with in vivo events and then to focus on those relevant assays in our studies of immunologic escape mechanisms. We also intend to examine effector mechanisms by fractionating cells and serum to determine wherein specific immunologic functions lie. Finally, we intend to examine the effects of progressive tumor growth and various therapeutic manipulations including excision, radiation therapy, chemotherapy, endocrine therapy and immunotherapy on immunologic escape mechanisms. It is our intention ultimately to apply the information gained from the R3327 model to patients with prostatic carcinoma.